Factors Affecting the Distribution of Neural Blockade by Local Anesthetics in Epidural
Anesthesia and a Comparison of Lumbar Versus Thoracic Epidural Anesthesia
Author(s):
Visser, W Anton MD, PhD*; Lee, Ruben A. BE(Hons)†; Gielen, Mathieu
J. M. MD, PhD‡
Issue:
Volume 107(2), August 2008, pp 708-721
Publication
[Analgesia: Regional Anesthesia: Review Article]
Type:
Publisher: © 2008 by International Anesthesia Research Society.
From the *Department of Anesthesiology, Intensive Care and Pain
Management, Amphia Hospital, Breda; †Department of Biomechanical
Engineering, Faculty of Mechanical, Maritime, and Materials
Engineering, Technical University of Delft, Delft; and ‡Department of
Anesthesiology, University Medical Center Nijmegen, Nijmegen, The
Netherlands.
Institution(s):
Reprints will not be available from the authors.
Accepted for publication April 18, 2008.
Address correspondence to W. Anton Visser, MD, Department of
Anesthesiology, Intensive Care and Pain Management, Amphia
Hospital, PO Box 90157, 4800 RL Breda, The Netherlands. Address email to avisser@amphia.nl.
Abstract
The spread of sensory blockade after epidural injection of a specific dose of local
anesthetic (LA) differs considerably among individuals, and the factors affecting this
distribution remain the subject of debate. Based on the results of recent
investigations regarding the distribution of epidural neural blockade, specifically for
thoracic epidural anesthesia, we noted that the total mass of LA appears to be the
most important factor in determining the extent of sensory, sympathetic, and motor
neural blockade, whereas the site of epidural needle/catheter placement governs
the pattern of distribution of blockade relative to the injection site. Age may be
positively correlated with the spread of sensory blockade, and the evidence is
somewhat stronger for thoracic than for lumbar epidural anesthesia. Other patient
characteristics and technical details, such as patient position, and mode and speed
of injection, exert only a small effect on the distribution of sensory blockade, or
their effects are equivocal. However, combinations of several patient and technical
factors may aid in predicting LA dose requirements. Based on these results, we have
also formulated suggested epidural insertion sites that may optimize both analgesia
and sympathicolysis for various surgical indications.
The spread of sensory blockade after epidural injection of a specific dose of local
anesthetic (LA) differs considerably among individuals, and the factors affecting this
distribution remain the subject of debate. Reviews on the subject date back two
decades or more.1,2 A systematic review of recent investigations may provide new
insights into factors that affect the spread of epidural blockade, especially for
thoracic epidural anesthesia, and may aid in delivering predictable and safe epidural
anesthesia.
Although previous reviews have focused primarily on lumbar epidural anesthesia, the
practice of thoracic epidural anesthesia has increased tremendously over the last
decade.3,4 Differences in anatomy, physiology, and techniques to identify the
epidural space make extrapolation of data for predicting spread of anesthesia
gathered during lumbar epidural anesthesia to thoracic epidural anesthesia
problematic. This article reviews recent investigations regarding the distribution of
neural blockade, specifically for thoracic epidural anesthesia and, where possible,
draws results from research regarding lumbar epidural anesthesia.
For the purpose of this review, we will consider C7–T2 as high-thoracic, T2–6 as midthoracic, and T6–L1 as low-thoracic. This classification reflects the different fields of
surgery for which these epidural sites are typically used (cardiac, thoracic and
abdominal surgery, respectively). In addition, most studies mentioned in this article
have used either LA, or contrast medium, or both, to study the distribution of
epidural anesthesia. However, it should be noted that the findings based on the use
of contrast medium may not always be congruent to epidural spread of LA.1,5,6
Although this review will focus on distribution of sensory neural blockade,
distribution of sympathetic and motor neural blockade will be briefly discussed.
A comprehensive description of epidural anatomy is beyond the scope of this article.
The reader is referred to several excellent reviews.7–10 In addition, methods used to
test sensory block have been reviewed elsewhere.11 These methods can be
categorized as either qualitative (normal or abolished response to the application of
stimuli such as cold or pinprick) or quantitative (e.g., pain on electrical stimulation
with increasing current). It should be noted that studies mentioned in this review
have used different modes of sensory testing, and that demonstration of blockade
using qualitative testing does not guarantee adequate anesthesia. It should also be
noted that, in general, surgical anesthesia has been the focus of investigations
concerning bolus doses of LA, whereas postoperative analgesia has been the focus in
evaluations regarding continuous infusions.
FACTORS AFFECTING THE DISTRIBUTION OF EPIDURAL NEURAL BLOCKADE
Patient Characteristics
Many studies have investigated patient characteristics to determine differences in
spread of neural blockade in epidural anesthesia. Although different factors are
examined separately in this review, multivariable analysis has shown that
consideration of multiple patient characteristics may better reflect the crossdependencies, and lead to a more accurate estimate of anesthetic requirements.12
Age
From the 1960s onward, the clinical impression that spread of epidural blockade may
be greater in elderly patients has spawned a host of studies investigating this
subject. In lumbar epidural anesthesia, Bromage was the first to report a strong
correlation between patient age and the epidural segmental dose requirements.13
However, the validity of these findings has been questioned, as the assumption of
linearity between LA dose and extent of anesthesia has later been proven to be a
fallacy (see below).1 Nevertheless, since then, several authors have reported
sensory blocks with maximum cephalad spread 3–8 segments higher in patients >60yr old compared to patients <40-yr old after injection of the same epidural dose of
LA.14–17 A linear relationship between age and spread of blockade is stronger when
using volumes up to 10 mL compared to the 10–20 mL range 14,18 and in patients
younger than 40 yr, compared to patients over 40-yr old.12,14 In a study comparing
the spread of sensory blockade in high-thoracic, mid-thoracic and lumbar epidural
anesthesia, correlation coefficients of spread with age in these three regions were
reported to be 0.58, 0.38, and 0.82, respectively.19 In contrast, other studies have
reported either no effect of age on epidural spread,20–22 or statistically significant,
but small correlation coefficients, with differences in spread of sensory blockade
that may not be clinically important.18,23–26
In contrast with the conflicting reports on lumbar epidural anesthesia, the few
studies investigating the effects of age on epidural spread in thoracic epidural
anesthesia all suggest a positive correlation between age and spread of blockade.
The epidural dose requirement in the elderly (60–79 yr) was demonstrated to be
about 40% less than in young adults (20–39 yr).27 This study demonstrated a
correlation coefficient between age and epidural dose requirement of -0.70 (Fig. 1).
Low thoracic epidural test doses of lidocaine 2%, 5 and 8 mL, resulted in greater
extent of blockade, smaller segmental dose requirements and an increased incidence
of hemodynamic instability in patients aged 56–80 yr compared to patients aged 18–
51 yr.28 Furthermore, positive correlation of thoracic epidural spread of contrast
medium with the patient’s age has been reported.29,30
Figure 1. Relationship between age and epidural dose requirement of 2%
mepivacaine in thoracic (T9–10) epidural anesthesia (r = 0.70, P < 0.001, n = 62). D =
Dermatome. 27
The mechanism for a positive correlation reported by several investigators between
age and spread of blockade remains unclear. Although it has been suggested that this
correlation could be explained by decreased leakage of LA through the intervertebral
foramina in older patients,31–34 this has been refuted by others.30 Alternatively,
compliance of the epidural space has been shown to increase with age, and it is
positively correlated with spread of sensory blockade.35 This agrees with the fact
that residual pressure after injection of LA is lower in older patients, which, in turn,
is associated with wider spread of sensory block.19 Indeed, it has been demonstrated
using epiduroscopy that the epidural space becomes more widely patent after
injection of a given amount of air, and the fatty tissue in the epidural space
diminishes with increasing age, which may promote the longitudinal spread of LAs in
the elderly.36 Furthermore, with age, the dura becomes more permeable to LA
owing to a progressive increase in size and number of arachnoid villi. This provides a
large area through which LA can diffuse into the subarachnoid space.34 Finally, it
has been proposed that a decrease in the number of myelinated nerve fibers in the
nerve, and a general deterioration of the mucopolysaccharides of the ground
substance, allows LA to more easily penetrate nerve roots in older patients.13,37
Height
It seems logical to assume that taller patients require more LA to establish a certain
level of blockade than shorter subjects. This has been investigated in lumbar
epidural anesthesia, again with conflicting results. Only weak correlation
coefficients, ranging from -0.13 to -0.54 have been demonstrated.18,20,24,38 In
thoracic epidural anesthesia, correlation coefficients from -0.25 29 to -0.37 30 have
been found between the spread of epidurally injected contrast medium and patient
height. To our knowledge, clinical trials evaluating the relationship between height
and spread of blockade after epidural administration of LA are lacking in thoracic
epidural anesthesia. Therefore, it is not possible to definitively draw conclusions on
the significance of patient height in predicting the spread of blockade, except
perhaps in extremely short or extremely tall individuals.
Weight and Body Mass Index
Few studies report on the correlation between weight and spread of sensory
blockade. In lumbar epidural anesthesia, no correlation was found,20,22 although a
correlation coefficient of 0.41 was demonstrated for the association of body mass
index (BMI) with height of sensory block.20 Weight was not correlated with epidural
spread of contrast in thoracic epidural anesthesia.29
Apparently, changes that may occur with obesity, such as increased abdominal
pressure or increased body fat, are not sufficient to affect the spread of epidural
blockade. Indeed, while both weight and BMI are positively correlated with posterior
subcutaneous body fat deposition, they are not or only poorly correlated with the
amount of posterior epidural fat.39
Pregnancy
Due to the lack of studies involving thoracic epidural anesthesia during pregnancy,
data on epidural anesthesia in pregnancy concern lumbar epidural anesthesia only. In
general, less LA is required to produce a given level of epidural anesthesia in
pregnant patients. Engorgement of epidural veins by increased intra-abdominal
pressure has often been implied as the mechanism for this phenomenon.
Furthermore, both animal 40–42 and clinical studies 43 have shown that during
pregnancy, onset of blockade of nerve conduction by LA is faster and blockade is
more intense. This may account for the appearance of increased spread of epidural
blockade during early pregnancy (8–12 wk) when intra-abdominal pressure is
probably still normal, which is similar to that found in pregnant women at term.44 In
contrast, no difference in latency and density of motor and sensory blockade was
found when tested with repeated electrical stimulation between pregnant and
nonpregnant women receiving lumbar epidural anesthesia.45 Although cranial
extension of blockade was higher in the pregnant group, onset of sensory block in
the sacral segments was similar in both groups. In contrast to the general population
(see above), epidural LA requirements are further reduced in obese parturients (BMI
>30) compared to parturients with BMI <=30.46
Dural Surface Area
It has been demonstrated that the surface area of the lumbosacral dura is correlated
with the peak sensory block level in lumbar epidural anesthesia.47 Although this
patient factor may not be clinically useful, future research in this area may further
clarify the differences in epidural spread of LAs among patients.
Technical Factors
Choice of Epidural Insertion Site
The length of the lumbar section of the vertebral column is relatively short and the
dimensions of the lumbar epidural space are fairly constant. Although statistically
significant, only small differences in cranial spread of blockade have been
demonstrated after injection of LA at three different lumbar interspaces.12 In
contrast, the thoracic part of the spinal column encompasses more than half the
length of the entire spine and adjoins many different anatomical structures and
spaces, whereas the thoracic vertebrae and epidural space vary greatly in shape and
size. Therefore, it may be speculated that the distribution of neural blockade may
vary with the site of epidural injection.
It is alleged that dose requirements are larger in lumbar compared to thoracic
epidural anesthesia. Interestingly, while this has also been suggested in several
papers,1,2,18 surprisingly few studies have actually directly compared the
differences in spread of blockade between lumbar and thoracic epidural anesthesia.
No statistically significant differences in total numbers of segments blocked could be
demonstrated after high-thoracic, mid-thoracic, low-thoracic or lumbar epidural
injection of contrast medium (Fig. 2).29,48 Others have reported spread of blockade
of 17.3 ± 0.6, 14.3 ± 0.4, and 13.3 ± 0.7 segments after injection of 15 mL of 2%
mepivacaine in the cervical, thoracic and lumbar epidural space, respectively.19
Unfortunately, these data were not statistically analyzed.
Figure 2. A: Extension of sensory blockade tested by pinprick after administration of
3 mL lidocaine 2% in the high (C7–T2), mid (T2–4) or low (T7–9) thoracic epidural
space. Data represent means ± sd. Arrows indicate the level of epidural needle
placement. 48 B: Mean contrast spread after injection of 5 mL iotrolan, 240 mg
I/mL, in 90 patients. C = cervical segment; L = lumbar segment; S = sacral segment;
T = thoracic segment. In this study, there was a strong correlation between
radiographic and analgesic spread (r = 0.91–0.97).29 These figures illustrate two
important issues in epidural anesthesia: First, in contrast to common teaching, no
statistically significant differences in total number of segments blocked could be
demonstrated between patients receiving cervical, high, mid-, or low-thoracic or
lumbar epidural injections. Second, the intervertebral level of epidural injection is a
statistically significant factor in the distribution of sensory blockade, either in the
cranial or caudal direction relative to the injection site.
Different patterns of sensory blockade were found after a test dose of 3 mL of
lidocaine 2% when injected at different sites in the thoracic epidural space. Spread
of sensory blockade was primarily caudal after high-thoracic epidural injection,
primarily cephalad after low-thoracic injection, and equally distributed caudal and
cephalad after mid-thoracic injection (Fig. 2A).48 These patterns have been
confirmed in a series of 90 patients receiving 5 mL of lidocaine 1.5% at vertebral
levels ranging from C7 to L5 (Fig. 2B).29 Differences in epidural pressure (see
below), and obstruction of spread of epidural LA by the larger relative volume of the
spinal cord and the thecal sac in the cervical and high lumbar areas have been
suggested as an explanation for this phenomenon.48 Also, epiduroscopy has shown
that the mid-thoracic epidural space becomes more widely patent after injection of
a given amount of air and that the amount of fatty and fibrous tissue is smaller
compared to the upper lumbar epidural space.49 Greater cranial spread (up to C2–3)
after epidural injection at the C7–T1 level has been reported when larger doses of LA
are being used. However, even in this situation, caudal spread is more extensive
than cranial spread.50–52 Despite the differences in spread of blockade in relation to
the site of injection, no differences were found in the total number of segments
blocked among different regions in the thoracic epidural space,29,48 indicating that
it is safe to use the same initial dose of LA in high- thoracic, mid-thoracic and lowthoracic epidural anesthesia.
Patient Position and Gravity
In lumbar epidural anesthesia, epidural injection of LA with the patient in the lateral
position produces sensory block levels approximately 0–3 segments greater on the
dependent side compared to injection with the patient in the supine position.21,53–
60 No differences have been reported in maximal cranial spread between groups
receiving equal amounts of epidural LA in the sitting or supine position.21,22,61
Some of these studies report slightly faster onset times in the lateral or sitting
positions compared to the supine position.22,53,54,60
Head down (Trendelenburg) position of 15° has been shown to result in higher
sensory block levels with faster onset times after lumbar epidural injection of LA in
pregnant women.62 There has been one case report in which a high epidural block
was diagnosed in an elderly patient, which made mechanical ventilation necessary.
This patient had received a continuous epidural infusion through a low-thoracic
epidural catheter, while positioned in a 15° head down lithotomy position for 4.5
h.63
Once again, studies on the effects of patient position and gravity in thoracic epidural
anesthesia are lacking. However, with regard to position only, it has recently been
shown that high-thoracic (catheter tip at T1–2) epidural injection of contrast
medium with the patient’s neck in extension or neutral position results in limited
cranial spread, whereas significant cranial spread was observed in patients after
injection with the neck flexed.64
Needle Direction and Catheter Position
Epidural injection through a Tuohy needle with the bevel oriented to one side 1 or
caudal 65,66 has no or only minor effects on the spread of sensory blockade
compared to injection directed cephalad. However, both in lumbar 67,68 and
cervical 69 epidural anesthesia, threading an epidural catheter with the Tuohy
needle rotated 45° toward the operative side has been shown to produce a
preferential distribution of sensory and motor blockade toward this side. In pregnant
women, insertion of an epidural catheter with the bevel of the Tuohy needle
oriented laterally resulted in greater difficulty passing the catheter and, more
frequently, paresthesia.70 In contrast with the reports mentioned above, no
differences were noted in the incidence of asymmetric block.
Orienting the bevel of the Tuohy needle caudad or cranially does not reliably predict
final lumbar 71 nor thoracic 48,72,73 epidural catheter position relative to the
insertion site. Also, thoracic epidural catheters have been shown to progressively
withdraw an average of 1 cm during the first 3 days after insertion.73 The optimal
distance to advance a catheter into the lumbar epidural space is suggested to be 4–6
cm.74,75 Threading shorter or longer distances may result in inadequate analgesia or
increased incidence of venous cannulation and frequency of paresthesias,
respectively.74,75 Fortunately, computed tomography imaging and clinical
experience demonstrate that a large variety of lumbar epidural catheter tip
positions and solution distribution result in equally satisfactory epidural
anesthesia.76
Injection Through Needle Versus Injection Through Catheter
Whether injection of LA through a Tuohy needle versus an epidural catheter yields
differences in epidural spread remains controversial. Lumbar epidural bolus injection
of LA via either a Tuohy needle or a catheter did not result in differences in epidural
spread in patients undergoing cesarean delivery 77 or lower extremity surgery.78 In
contrast, injection of 14 mL lidocaine 2% through a lumbar epidural catheter
resulted in a spread of sensory blockade four segments greater compared to
injection at the same rate through a Tuohy needle.79 Another study comparing these
two modes of injection in pregnant women reported better quality of anesthesia
when LA was injected via an epidural catheter.80 However, injection times differed
by a factor of three between groups, which may have affected the results. We are
unaware of similar studies in thoracic epidural anesthesia.
Epidural Catheter Design
Epidural catheters may be categorized as either single-orifice or multiorifice designs.
In vitro, using injection pressures derived from in vivo measurements, differential
flow has been observed from multiorifice epidural catheters, i.e., the flow appears
first at the proximal, then the middle, and finally the distal orifices.81 With low
injection pressures, flow is largest from the proximal orifice, and no flow was
observed from the distal orifice, rendering a multiorifice catheter effectively a
single-orifice variant.
Comparisons between these two catheter designs are commonly presented as
differences in the quality of analgesia, rather than differences in spread of sensory
blockade. In this regard, multiorifice catheters have been shown to be superior to
single-orifice catheters in obstetric lumbar epidural anesthesia.82–84 In particular,
unilateral analgesia and unblocked segments are reported to occur more frequently
when a single-orifice catheter is placed.84 In contrast, one study did not find any
differences in the quality of analgesia between single- and multiorifice catheters.85
Furthermore, injection of contrast medium resulted in a similar number of segments
covered by dye above and below the injection site with both catheter designs.86
With newer soft-tipped single-orifice catheters, the lower incidence of paresthesias
and venous cannulation during placement should be weighed against the higher
incidence of inadequate or unilateral analgesia associated with this type of
catheter.87,88 We are unaware of any studies comparing different designs of
multiorifice catheters (e.g., longitudinal versus circumferential alignment of
orifices).
Fractional Versus Single Bolus Injection
Administration of a specified dose of LA may result in different spread of blockade
when injected as a single bolus compared to giving the same dose in smaller
fractions.89 In low-thoracic epidural anesthesia, the effect of timing of fractionated
doses of LA on the spread of sensory blockade has been investigated. Administration
of two doses of 5 mL of LA with an interval of 5 min produced an epidural block of
similar extent as a single injection of 10 mL of LA. However, with an interval of 10
min, the number of segments blocked was smaller compared to the two other modes
of injection mentioned.89 The authors suggested that differences in residual
epidural pressures (see below) may explain these differences. Also, prior injection of
large volumes (5–10 mL) of saline, e.g., when the loss-of-resistance technique is
used, may result in a greater spread of neural blockade after injecting LA.90
However, this phenomenon has only been observed using mepivacaine 1.5% and not
when using mepivacaine 1%, indicating that dilution of the higher concentration by
saline may also contribute.90 Also, this effect is exaggerated when the interval
between both injections is short.91 We are unaware of similar studies in lumbar
epidural anesthesia.
Speed of Injection
In lumbar epidural anesthesia, only one study has reported a positive correlation
between speed of injection and cranial spread of blockade: Injection through a
Tuohy needle of 14 mL lidocaine 2% at a rate of 1.2 mL/s resulted in a spread of
sensory blockade four segments greater compared to injection at a rate of 0.24
mL/s.79 In contrast, rapid injection of mepivacaine 8 mL in 8 s versus 160 s resulted
in the same number of dermatomes blocked after 15 min.92 However, onset of
blockade was more rapid in the fast injection group. The number of patients with
perineal blockade after 5 min was more than four times higher in the fast injection
group compared to the slow injection group. A similar number of dermatomes
blocked or maximum cranial level of blockade after 30 min with 66,93 or without
faster onset 55 has also been reported by other investigators. Whether speed of
injection may exert its effect on the spread of blockade through changes in epidural
pressure remains controversial (see below).
Epidural Pressures and Pressures in Adjacent Body Cavities
Epidural Pressures
Pressure gradients within the epidural space, and between this space and adjacent
body cavities may play a role in the distribution of LA injected in the thoracic
epidural space.31,48 Since sensory block after both low-thoracic and high-thoracic
epidural injection of lidocaine spreads from the site of injection toward the midthoracic epidural space,29,48,64,94 it has been suggested that the latter may harbor
a lower pressure.48 This may facilitate spread of LA toward the mid-thoracic
epidural space. Indeed, a small, but statistically significant, difference in epidural
pressure has been demonstrated, with the mid-thoracic epidural pressure being
slightly lower than the low-thoracic epidural pressure.95 Also, in this study, subatmospheric pressure was observed more frequently in the mid-thoracic compared to
the low-thoracic epidural space. It is difficult to compare studies evaluating epidural
pressures because of the many differences in study design, definition of epidural
pressure, and lack of homogeneity in the populations studied. It should be noted that
debate continues whether epidural pressure is positive or negative (with regard to
atmosphere), and whether the pressures reported are true pressures or artifacts.96
Epidural pressure has been found to be positive by some authors,95,97–99 but
slightly negative by others.31,96,100,101 In light of the pressures generated by
epidural injection,102 it remains to be investigated whether pressure gradients
within the epidural space are sufficient to influence spread of LA. Lumbar epidural
pressure after epidural injection of LA may be correlated to the spread of sensory
block. However, both positive 19,31,35 and negative 55,102,103 correlations have
been reported.
Pressures in Adjacent Body Cavities
Since the epidural space is continuous (or contiguous) with many other body cavities,
pressures in these cavities may also influence the spread of sensory blockade. The
difference in patency after a given amount of injected air between the thoracic and
lumbar epidural spaces, as seen by the epiduroscope, may be influenced by the
negative intrapleural and positive intra-abdominal pressures.36 Increasing airway
pressure using a continuous positive airway pressure (CPAP) device increases the
number of segments blocked after a low-thoracic epidural injection of lidocaine by
57%, primarily through a more caudad spread of the block.104 Furthermore, a more
cranial extension of sensory blockade was demonstrated after cervico-thoracic (C6–7
or C7–T1) epidural injection of lidocaine in patients breathing on CPAP.105
Therefore, when airway pressure is increased by the application of CPAP, the distal
border of sensory blockade extends further away from the thorax, i.e., more
cranially after high-thoracic injection,105 and more caudad after low-thoracic
injection.104 Although speculative, a similar effect may occur during positive
pressure ventilation in anesthetized patients.104
Alteration of epidural pressure by CPAP has not been confirmed.104 Although
pneumoperitoneum during laparoscopic procedures 106 and ventilation with positive
end-expiratory pressure 107 have been shown to increase epidural pressure, there
are no studies that have investigated the effects of these maneuvers on the spread
of epidural blockade.
Local Anesthetics
Total Dose, Concentration Versus Volume
Overall, the amount of LA injected influences the spread of epidural blockade.
However, the notion that increasing the dose of LA results in a linear increase in the
spread of blockade 13 has often been questioned. Although there may be such a
linear relationship in patients younger than 40 yr,14 in patients of 50 yr and older,
the relationship between dose and number of segments blocked is dependent on the
volume previously injected, i.e., the higher the volume already injected, the higher
the dose requirement to block an additional segment (Fig. 3).14,21,23,108 Indeed, a
linear relationship between subsequent segmental dose requirements and dose
previously injected has been described.14,21,108 Given this complex relationship
between LA dose and sensory blockade, formulas that have been proposed to predict
segmental dose requirements of LA are equally complex.108 However, simpler
formulas derived from cubic polynomial equations have been validated in clinical
practice.109
Figure 3. Scattergram and cubic polynomial fit between injected volume of 2%
mepivacaine and number of anesthetized dermatomes. This figure illustrates the
observation that the spread of epidural anesthesia changes proportionally more after
a small volume of local anesthetic is administered than after a larger dose is
given.122
Many studies have compared the effects of administering equal doses of LA, in
solutions with different concentrations. The conclusion that the same total mass of
drug given in different concentrations and volumes produces similar spread of
sensory blockade and equally effective analgesia is widely supported in lumbar
epidural anesthesia for bolus injections.2,20,110 In thoracic epidural anesthesia, this
has been demonstrated both for single bolus injection 48,111 and for continuous
epidural infusion.112–115 However, some authors have reported cranial block levels
2–4 segments higher with low concentrations compared to higher concentrations of
LA, without differences in quality of analgesia or incidence of motor block.116–119
Others have reported better analgesia with higher volumes of LA.120 Although
administration of the same mass of LAs in different volumes results in similar spread
of neural blockade, the intensity of blockade may vary with the concentration of LA.
Differences in intensity of sensory blockade using cutaneous electrical stimulation
between groups receiving equal amounts of LA in different volumes have both been
confirmed 121 and refuted.119 Most reports on perioperative epidural analgesia
using bupivacaine have studied concentrations ranging from 0.1% to 0.5%. Since all
studies mentioned above report equally satisfactory analgesia using different
combinations of volume and concentration, the potential difference in intensity of
blockade appears not to be clinically relevant.
It has been demonstrated that 2% lidocaine diluted with the same volume of saline
produces less potent epidural blockade, in terms of number of segments blocked and
achievement of perineal blockade, than commercially prepared 1% lidocaine.122
This may be explained by differences in the concentrations of sodium, chloride,
hydroxide, and hydrogen ions.122
Additives to Local Anesthetics
Bicarbonate
An increase in pH by adding bicarbonate to a solution of LA results in an increase in
the nonionized fraction of the LA and improved nerve penetration.123,124 Adding
bicarbonate increases the pain threshold in blocked dermatomes,125–127 increases
the depth of motor block,127 and reduces the time to onset of blockade of the first
sacral segment.127 In contrast, spread of sensory blockade as evaluated by pinprick
is not affected,126,127 however, the sample sizes in these studies were based on
pain threshold data and may have been too small to demonstrate a difference in
spread of blockade.
[alpha]2 Agonists and Opioids
Stimulation of [alpha]2 receptors located in the spinal cord produces
antinociception.128 Both epinephrine and clonidine produce segmental
hypoalgesia.129 The addition of [alpha]2 agonists to LA results in faster onset and
longer duration of sensory and motor blockade,130 decreased plasma LA levels,131
and improved intraoperative anesthetic quality.131 However, spread of sensory
block has been shown to be similar after injection of levobupivacaine alone, or with
various amounts of epinephrine.131
Opioids exert their spinal analgesic effects at the level of the dorsal horn.132
Whether epidurally injected opioids produce analgesia through a spinal or supraspinal mechanism or both,132,133 is beyond the scope of this article. However, it is
clear that the synergistic action 134,135 between these two types of drugs allows a
reduction in the dose and side effects of both LA and opioid, while enhancing the
degree of pain relief. Adding opioids to epidural LA has been shown to hasten the
onset, but not affect the spread of sensory blockade.136 No difference in extent of
sensory blockade was demonstrated between groups receiving epidural bupivacaine
with sufentanil added epidurally versus IV,137 whereas consumption of sufentanil in
the epidural group was half that of the IV group. However, since sample size was
based on sufentanil consumption, this study may have been under-powered to
demonstrate a difference in spread of blockade.
Sympathetic Block
Over the last 10–15 yr, epidural sympathetic neural blockade has been recognized for
its potential to improve outcome in cardiac 138 and colorectal surgery.139
Sympathicolysis of the cardiac acceleration fibers (T1–4) may contribute to improved
cardiac oxygen balance and decreased biochemical markers of perioperative cardiac
ischemia,138 whereas blockade of the splanchnic sympathetic nerves (T6–L1) may
protect against perioperative intestinal ischemia,140 and is associated with quicker
return of bowel function and general recovery.139 Indeed, a future therapeutic role
for low-thoracic epidural anesthesia has been suggested in the treatment of septic
shock.140
Despite the possible presence of a small zone of differential block, spread of
sympathetic blockade generally follows the same patterns as sensory
blockade.141,142 Using changes in regional skin temperature in the lower
extremities as an indirect indicator of diminished efferent sympathetic nerve
activity, both animal 143 and human 144 studies have indicated that the sympathetic
blockade associated with segmental high-thoracic epidural anesthesia may extend
caudally beyond the area of sensory blockade. However, the change in foot skin
temperature is much smaller compared to that induced by lumbar epidural
anesthesia.144 Furthermore, direct techniques, such as muscle and skin sympathetic
nerve activity measurements with microelectrodes, have shown no inhibition of
resting sympathetic nerve activity to the lower extremities by thoracic epidural
anesthesia limited to the upper thoracic dermatomes.145 Conversely, lumbar
epidural anesthesia induces compensatory vasoconstriction 146 and increased
cardiac sympathetic nerve activity 147 in unblocked segments. Therefore, when
epidural anesthesia is to be used for both its analgesic and sympathicolytic effects,
both these effects should be considered when selecting the site of epidural
placement. This means, for example, that to provide complete blockade of the
cardiac acceleration fibers, high-thoracic epidural anesthesia should be selected,
and to block the splanchnic sympathetic system, low-thoracic epidural anesthesia
should be used (Table 1).29,48
Table 1. Recommendations for Epidural Catheter Insertion Site
Degrees of sympathetic blockade in clinical studies are most often derived from
changes in hemodynamic variables, e.g., arterial blood pressure, heart rate or
cardiac output. These cardiovascular sequelae of epidural anesthesia have been
reviewed elsewhere.141 Specifically, factors that are positively correlated with the
occurrence of hypotension and bradycardia during lumbar epidural anesthesia
include increasing body weight, spread of sensory blockade, and the addition of
fentanyl to the LA.148 In high-thoracic epidural anesthesia, no changes in
hemodynamic variables were observed when comparing equal volumes of 0.25%
bupivacaine to 0.375% in a crossover design.51
Motor Block
One of the attractive features of thoracic compared to lumbar epidural anesthesia is
its lack of significant motor block of the lower extremities. However, motor block of
the phrenic nerve and both upper and lower extremities can occur in thoracic
epidural anesthesia, depending on the insertion site.
Phrenic Nerve Motor Block
Phrenic nerve function has been studied in patients receiving cervico-thoracic
epidural anesthesia. Injection of 3 105 or 15 mL 52 of 2% lidocaine at the C7–T1
interspace resulted in only mild changes in pulmonary function as measured by
forced expiratory volume in 1 min, forced vital capacity and maximum inspiratory
pressure. In contrast, using the same variables and epidural catheters placed at the
same interspace, a clinically important impairment of pulmonary function was
observed in a concentration-dependent manner after injection of both bupivacaine
0.25% or 0.375 50 and lidocaine 0.5%, 1% and 2%.149 In an older study, inspiratory
capacity, vital capacity, total lung capacity, and forced expiratory volume in 1 min
were reduced by thoracic epidural anesthesia using 10 mL of mepivacaine 2% at both
the C7–T1 and T12–L1 levels.150 These changes were significantly greater with highthoracic compared to low-thoracic epidural anesthesia. In contrast, functional
residual capacity decreased after low-thoracic, but not after high-thoracic epidural
anesthesia. Changes in Po2 and Pco2 were only minor. The authors concluded that
motor block of both the diaphragm and the intercostal muscles may play a role in
the ventilatory changes.
Upper Extremity Motor Block
A concentration-dependent decrease of hand strength has been demonstrated in
cervico-thoracic epidural anesthesia.50 Mild hand weakness occurred in 16% of
patients receiving continuous high-thoracic epidural anesthesia for cardiac
surgery.151 Using a scoring scale for arm movements, decreased upper extremity
motor function was demonstrated in 30% of patients with epidural catheters between
C7 and T4.152 Indeed, this scale has been proposed to serve as a simple and reliable
method for the early detection of cephalad spread of thoracic epidural anesthesia,
before this affects phrenic nerve function.152
Lower Extremity Motor Block
Some degree of lower extremity motor block is common in lumbar epidural
anesthesia. With continuous infusion of LA, increasing degrees of motor blockade
have been reported with increasing infusion rates while the concentration of the LA
is held constant,153 or when the concentration of LA is increased while the infusion
rate is held constant.115,154 Therefore, similar to the spread of sensory blockade,
total mass of LA appears to be the most important factor concerning the degree of
lower extremity motor block. This has been confirmed in volunteers receiving
different concentrations and volumes of equal doses of LA.119 Adding opioids to the
LA accelerates the onset of motor blockade in lumbar epidural anesthesia.136 The
intensity of motor block is not influenced by the speed of epidural injection,92
whereas it is increased when bicarbonate is added to the LA 127 and in older
patients.15,25,26,155 The decrease in conduction velocity in older patients affects
motor nerves in particular,37 which may explain why there is less controversy on the
effect of age on motor blockade compared to the effect of age on sensory blockade.
Lumbar epidural injection in the lateral position results in more profound motor
block on the dependent side.18,60 While not a clinically useful variable, posterior
epidural fat volume is inversely correlated with the degree of motor block.47
In thoracic epidural anesthesia, lower extremity motor block can often be avoided,
or is present in only mild degrees.113,114,116–118,156 A high concentration of LA in
a low volume may cause less motor block to the lower extremities in thoracic
epidural anesthesia,114 although this could not be confirmed in other studies by the
same 117 and other authors.156 Placement of catheters in proximity to lumbar
spinal segments increases the risk of motor block when compared to a more
cephalad placement.117,157,158 The severity of lower extremity motor block in
thoracic epidural anesthesia may also be decreased by using patient-controlled
epidural analgesia instead of continuous infusion of LA, as this results in smaller
amounts of drugs used, while maintaining equally satisfactory levels of
analgesia.113,156,159
CONCLUSION
Factors Affecting the Distribution of Epidural Block
Distribution of sensory blockade after epidural injection of LA varies widely among
individuals, and may only be partially predicted based upon known factors. Based on
this review, the total mass of LA appears to be most important factor in determining
the extent of sensory, sympathetic, and motor neural blockade, while the site of
epidural needle/catheter insertion governs the pattern of distribution of sensory
blockade relative to the injection site. Age may be positively correlated with the
spread of sensory blockade, although the evidence is somewhat stronger for thoracic
than for lumbar epidural anesthesia. Other patient characteristics and technical
details such as patient position and mode and speed of injection have all been shown
to exert only a small effect on the distribution of sensory blockade, or their effects
are controversial. However, combinations of several patient and technical factors
may aid in predicting LA dose requirements. Also, maneuvers such as rapid injection,
placing the patient in the lateral position, or adding bicarbonate to LA solutions may
be applied to quicken the onset of blockade. The influence of the factors mentioned
above may be summarized in a semi-quantitative fashion as presented in Table 2.
Table 2. Summary of Factors Affecting the Spread of Epidural Neural Blockade
Selection of Epidural Insertion Site
It has been suggested that epidural catheters should be sited at an intervertebral
space that represents the middle of the area of surgical incision.115 However, we
feel this advice does not consider the different patterns of distribution after single
injection or continuous infusion of LA. Also, with the recent recognition of the
beneficial effects of sympathicolysis, sympathetic epidural blockade in a particular
area of the body may be considered as important as satisfactory analgesia. Based on
this review, we have formulated suggested epidural insertion sites for various
surgical indications that may serve to accomplish both goals (Table 1).
ACKNOWLEDGMENTS
The authors thank Dr. André van Zundert and Dr. Quinn Hogan for critically
reviewing and discussing earlier versions of the manuscript.
REFERENCES
1. Park WY. Factors influencing distribution of local anesthetics in the epidural
space. Reg Anesth 1988;13:49–57 [Context Link]
2. Bromage PR. Mechanism of action of extradural analgesia. Br J Anaesth
1975;47:199–211 Bibliographic Links [Context Link]
3. Wheatly RG, Schug SA, Watson D. Safety and efficacy of postoperative epidural
analgesia. Br J Anaesth 2001;87:47–61 [Context Link]
4. Pennefather SH, Gilby S, Danecki A, Russell GN. The changing practice of thoracic
epidural analgesia in the United Kingdom: 1997–2004. Anaesthesia 2006;61:363–9
Ovid Full Text Bibliographic Links [Context Link]
5. Marret E, Gibert S, Bonnet F. Can epidurography help to predict the extent of
epidural blockade? Anesthesiology 2005;102:478–9 Ovid Full Text Bibliographic Links
[Context Link]
6. Slappendel R, Gielen MJM, Hasenbos MAWM, Heystraten FMJ. Spread of
radiopaque dye in the thoracic epidural space. Anaesthesia 1988;43:939–42
Bibliographic Links [Context Link]
7. Reina MA, De Andrés JA, Maches F, Lopez A. Anatomy of the epidural space and
new insights. Highlights in regional anaesthesia and pain therapy. Proceedings of the
25th Annual Meeting of the Eur Society of Regional Anaesthesia (ESRA), 2006
[Context Link]
8. Elizaga AM, ed. Illustrated notes in regional anesthesia. 1997. Available at
http://depts.washington.edu/anesth/regional/Page1.html [Context Link]
9. Hogan QH. Epidural anatomy: new observations. Can J Anaesth 1998;45:R40–R44
Bibliographic Links [Context Link]
10. Hogan QH. Lumbar epidural anatomy: a new look by cryomicrotome section.
Anesthesiology 1991;75:767–75 Buy Now Bibliographic Links [Context Link]
11. Curatolo M, Petersen-Felix S, Arendt-Nielsen L. Assessment of regional analgesia
in humans: a review of methods and applications. Anesthesiology 2000;93:1517–30
Ovid Full Text Bibliographic Links [Context Link]
12. Curatolo M, Orlando A, Zbinden AM, Scaramozzino P, Venuti FS. A multifactorial
analysis of the spread of epidural analgesia. Acta Anesthesiol Scand 1994;38:646–52
[Context Link]
13. Bromage PR. Exaggerated spread of epidural analgesia in arteriosclerotic
patients: dosage in relation to biological and chronological ageing. BMJ 1962;2:1634–
8 Bibliographic Links [Context Link]
14. Sharrock NE. Epidural anesthetic dose response in patients 20 to 80 years old.
Anesthesiology 1978;49:425–8 Bibliographic Links [Context Link]
15. Nydahl PA, Philipson L, Axelsson K, Johansson JE. Epidural anesthesia with 0.5%
bupivacaine: influence of age on sensory and motor blockade. Anesth Analg
1991;73:780–6 Ovid Full Text Bibliographic Links [Context Link]
16. Simon MJ, Veering BT, Stienstra R, van Kleef JW, Burm AG. The effect of age on
neural blockade and hemodynamic changes after epidural anesthesia with
ropivacaine. Anesth Analg 2002;94:1325–30 Ovid Full Text Bibliographic Links
[Context Link]
17. Finucane BT, Hammonds WD, Welch MB. Influence of age on vascular absorption
of lidocaine from the epidural space. Anesth Analg 1987;66:843–6 Ovid Full Text
Bibliographic Links [Context Link]
18. Grundy EM, Ramamurthy S, Patel KP, Mani M, Winnie AP. Extradural analgesia
revisited: a statistical study. Br J Anaesth 1978;50:805–9 Bibliographic Links [Context
Link]
19. Hirabayashi Y, Matsuda I, Sohzaburoh I, Shimizu R. Spread of epidural analgesia
following a constant pressure injection-an investigation of relationships between
locus of injection, epidural pressure and spread of analgesia. J Anesth 1987;1:44–50
Bibliographic Links [Context Link]
20. Duggan J, Bowler GM, McClure JH, Wildsmith JA. Extradural block with
bupivacaine: influence of dose, volume, concentration and patient characteristics.
Br J Anaesth 1988;61:324–31 Bibliographic Links [Context Link]
21. Andersen S, Cold GE. Dose response studies in elderly patients subjected to
epidural analgesia. Acta Anaesthesiol Scand 1981;25:279–81 Bibliographic Links
[Context Link]
22. Whalley DG, D’Amico JA, Rybicki LA, Gottlieb A, Ryckman JV, Schoenwald PK,
Bedocs NM. The effect of posture on the induction of epidural anesthesia for
peripheral vascular surgery. Reg Anesth 1995;20:407–11 Bibliographic Links [Context
Link]
23. Park WY, Hagins FM, Rivat EL, Macnamara TE. Age and epidural dose response in
adult men. Anesthesiology 1982;56:318–20 Buy Now Bibliographic Links [Context
Link]
24. Park WY, Massengale MD, Kim SI, Poon KC, Macnamara TE. Age and the spread of
local anesthetic solutions in the epidural space. Anesth Analg 1980;59:768–71 Ovid
Full Text Bibliographic Links [Context Link]
25. Veering BT, Burm AG, van Kleef JW, Hennis PJ, Spierdijk J. Epidural anesthesia
with bupivacaine: effects of age on neural blockade and pharmacokinetics. Anesth
Analg 1987;66:589–93 Ovid Full Text Bibliographic Links [Context Link]
26. Veering BT, Burm AGL, Vletter AA, van den Heuvel RP, Onkenhout W, Spierdijk J.
The effect of age on the systemic absorption, disposition and pharmacodynamics of
bupivacaine after epidural administration. Clin Pharmacokinet 1992;22:75–84 Buy
Now Bibliographic Links [Context Link]
27. Hirabayashi Y, Shimizu R. Effect of age on extradural dose requirement in
thoracic extradural anaesthesia. Br J Anaesth 1993;71:445–6 Bibliographic Links
[Context Link]
28. Holman SJ, Bosco RR, Kao TC, Mazzilli MA, Dietrich KJ, Rolain RA, Stevens RA.
What constitutes an effective but safe initial dose of lidocaine to test a thoracic
epidural catheter? Anesth Analg 2001;93:749–54 Ovid Full Text Bibliographic Links
[Context Link]
29. Yokoyama M, Hanazaki M, Fujii H, Mizobuchi S, Nakatsuka H, Takahashi T,
Matsumi M, Takeuchi M, Morita K. Correlation between the distribution of contrast
medium and the extent of blockade during epidural anesthesia. Anesthesiology
2004;100:1504–10 Ovid Full Text Bibliographic Links [Context Link]
30. Saitoh K, Hirabayashi Y, Shimizu R, Mitsuhata H, Fukuda H. Extensive extradural
spread in the elderly may not relate to decreased leakage through intervertebral
foramina. Br J Anaesth 1995;75:688–91 Bibliographic Links [Context Link]
31. Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and its relation to
spread of anesthetic solutions in the epidural space. Anesth Analg 1967;46:440–6
Ovid Full Text Bibliographic Links [Context Link]
32. Burn JM, Gruyer PB, Langdon L. The spread of solutions injected into the
epidural space: a study using epidurograms in patients with the lumbosciatic
syndrome. Br J Anaesth 1973;45:338–45 Bibliographic Links [Context Link]
33. Bromage PR. Tissue space connections. In: Bromage PR, ed. Epidural analgesia.
Philadelphia: WB Saunders, 1978:31–2 [Context Link]
34. Shanta TR, Evans JA. The relationship of epidural anesthesia to neural
membranes and arachnoid villi. Anesthesiology 1972;37:543–57 [Context Link]
35. Hirabayashi Y, Shimizu R, Matsuda I, Inowe S. Effect of extradural compliance
and resistance on spread of extradural analgesia. Br J Anaesth 1990;65:508–13
Bibliographic Links [Context Link]
36. Igarashi T, Hirabayashi Y, Shimizu R, Saitoh K, Fukuda H, Mitsuhata H. The
lumbar extradural structure changes with increasing age. Br J Anaesth 1997;78:149–
52 Bibliographic Links [Context Link]
37. Dorfman LJ, Bosley TM. Age-related changes in peripheral and central nerve
conduction in man. Neurology 1979;29:38–44 Bibliographic Links [Context Link]
38. Bromage PR. Spread of analgesic solutions in the epidural space and their site of
action: a statistical study. Br J Anaesth 1962;34:161–78 Bibliographic Links [Context
Link]
39. Wu HT, Schweitzer ME, Parker L. Is epidural fat associated with body habitus? J
Comput Assist Tomogr 2005;29:99–102 Buy Now Bibliographic Links [Context Link]
40. Datta S, Lambert DH, Gregus J, Gissen AJ, Covino BG. Differential sensitivities of
mammalian nerve fibers during pregnancy. Anesth Analg 1983;62:1070–2 Ovid Full
Text Bibliographic Links [Context Link]
41. Kaneko M, Saito Y, Kirihara Y, Kosaka Y. Pregnancy enhances the antinociceptive
effects of extradural lignocaine in the rat. Br J Anaesth 1994;72:657–61 Bibliographic
Links [Context Link]
42. Flanagan HL, Datta S, Lambert DH, Gissen AJ, Covino BG. Effect of pregnancy on
bupivacaine-induced conduction blockade in the isolated rabbit vagus nerve. Anesth
Analg 1987;66:123–6 Bibliographic Links [Context Link]
43. Butterworth JF, Walker FO, Lysak SZ. Pregnancy increases median nerve
susceptibility to lidocaine. Anesthesiology 1990;72:962–5 Buy Now Bibliographic Links
[Context Link]
44. Fagraeus L, Urban BJ, Bromage PR. Spread of epidural analgesia in early
pregnancy. Anesthesiology 1983;58:184–7 [Context Link]
45. Arakawa M. Does pregnancy increase the efficacy of lumbar epidural anesthesia?
Int J Obstet Anesth 2004;13:86–90 Bibliographic Links [Context Link]
46. Panni MK, Columb MO. Obese parturients have lower epidural local anaesthetic
requirements for analgesia in labour. Br J Anaesth 2006;96:106–10 Ovid Full Text
Bibliographic Links [Context Link]
47. Higuchi H, Adachi Y, Kazama T. Factors affecting the spread and duration of
epidural anesthesia with ropivacaine. Anesthesiology 2004;101:451–60 Ovid Full Text
Bibliographic Links [Context Link]
48. Visser WA, Liem TH, van Egmond J, Gielen MJM. Extension of sensory blockade
after thoracic administration of a test dose of lidocaine at three different levels.
Anesth Analg 1998;86:332–5 Ovid Full Text Bibliographic Links [Context Link]
49. Igarashi T, Hirabayashi Y, Shimizu R, Saitoh K, Fukuda H. Thoracic and lumbar
extradural structure examined by extraduroscope. Br J Anaesth 1998;81:121–5
Bibliographic Links [Context Link]
50. Capdevila X, Biboulet P, Rubenovitch J, Serre-Cousine O, Peray P, Deschodt J,
d’Athis F. The effects of cervical epidural anesthesia with bupivacaine on pulmonary
function in conscious patients. Anesth Analg 1998;86:1033–8 Ovid Full Text
Bibliographic Links [Context Link]
51. Biboulet P, Deschodt J, Capdevila X, Landreau L, Aubas P, du Cailar J, d’Athis F.
Hemodynamic effects of 0.375% versus 0.25% bupivacaine during cervical epidural
anesthesia for hand surgery. Reg Anesth 1995;20:33–40 Bibliographic Links [Context
Link]
52. Stevens RA, Frey K, Sheikh T, Kao TC, Mikat-Stevens M, Morales M. Time course
of the effects of cervical epidural anesthesia on pulmonary function. Reg Anesth Pain
Med 1998;23:20–4 Bibliographic Links [Context Link]
53. Grundy EM, Rao LN, Winnie AP. Epidural anesthesia and the lateral position.
Anesth Analg 1978;57:95–7 Ovid Full Text Bibliographic Links [Context Link]
54. Apostolou GA, Zarmakoupis PK, Mastrokostopoulos GT. Spread of epidural
anesthesia and the lateral position. Anesth Analg 1981;60:584–6 Ovid Full Text
Bibliographic Links [Context Link]
55. Husemeyer RP, White DC. Lumbar extradural injection pressures in pregnant
women: an investigation of relationships between rate of injection, injection
pressures, and extent of analgesia. Br J Anaesth 1980;52:55–60 [Context Link]
56. Park WY, Hagins FM, Macnamara TE. Lateral position and epidural anesthetic
spread. Anesth Analg 1983;62:278–9 [Context Link]
57. Preston R, Crosby ET, Kotarba D, Dudas H, Elliott RD. Maternal positioning
affects fetal heart rate changes after epidural analgesia for labour. Can J Anaesth
1993;40:1136–41 Bibliographic Links [Context Link]
58. Soetens FM, Meeuwis HC, van der Donck AG, de Vel MA, Schijven MP, van Zundert
AA. Influence of maternal position during epidural labor analgesia. Int J Obstet
Anesth 2003;12:98–101 Bibliographic Links [Context Link]
59. Shapiro A, Fredman B, Zohar E, Olsfanger D, Abu-Ras H, Jedeikin R. Alternating
patient position following the induction of obstetric epidural analgesia does not
affect local anaesthetic spread. Int J Obstet Anesth 1998;7:153–6 Bibliographic Links
[Context Link]
60. Seow LT, Lips FJ, Cousins MJ. Effect of lateral posture on epidural blockade for
surgery. Anaesth Intensive Care 1983;11:97–102 Bibliographic Links [Context Link]
61. Park WY, Hagins FM, Massengale MD, Macnamara TE. The sitting position and
anesthetic spread in the epidural space. Anesth Analg 1984;63:863–4 Ovid Full Text
Bibliographic Links [Context Link]
62. Setayesh AR, Kholdebarin AR, Saber Moghadam M, Setayesh HR. The
Trendelenburg position increases the spread and accelerates the onset of epidural
anesthesia for cesarean section. Can J Anaesth 2001;48:890–3 Bibliographic Links
[Context Link]
63. White N. Cephalad spread of epidural blockade in a 15-degree head-down
position. Anaesthesia 1999;54:1007–8 [Context Link]
64. Lee CJ, Jeon Y, Lim YJ, Bahk JH, Kim YC, Lee SC, Kim CS. The influence of neck
flexion and extension on the distribution of contrast medium in the high thoracic
epidural space. Anesth Analg 2007;104:1583–6 Ovid Full Text Bibliographic Links
[Context Link]
65. Park WY, Poon KC, Massengale MD, Macnamara TE. Direction of the needle bevel
and epidural spread. Anesthesiology 1982;57:327–8 Buy Now Bibliographic Links
[Context Link]
66. Rosenberg PH, Saramies L, Alila A. Lumbar epidural anaesthesia with bupivacaine
in old patients: effect of speed and direction of injection. Acta Anaesthesiol Scand
1981;25:270–4 Bibliographic Links [Context Link]
67. Borghi B, Agnoletti V, Ricci A, van Oven H, Montone N, Casati A. A prospective,
randomized evaluation of the effects of epidural needle rotation on the distribution
of epidural block. Anesth Analg 2004;98:1473–8 Ovid Full Text Bibliographic Links
[Context Link]
68. Dauri M, Sidiropoulou, Fabbi E, Mariani PP, Sabato AF. Intentional lateral
epidural catheter placement for anterior cruciate ligament reconstruction. Acta
Anaesthesiol Scand 2005;49:671–6 Buy Now Bibliographic Links [Context Link]
69. Buchheit T, Crews JC. Lateral cervical epidural catheter placement for
continuous unilateral upper extremity analgesia and sympathetic block. Reg Anesth
Pain Med 2000;25:313–7 Bibliographic Links [Context Link]
70. Richardson MG, Wissler RN. The effects of needle bevel orientation during
epidural catheter insertion in laboring parturients. Anesth Analg 1999;88:352–6 Ovid
Full Text Bibliographic Links [Context Link]
71. Tiso RL, Thomas PS, Macadaeg K. Epidural catheter direction and local
anesthetic dose. Reg Anesth 1993;18:308–11 Bibliographic Links [Context Link]
72. Choi DH, Lee SM, Cho HS, Ahn HJ. Relationship between the bevel of the Tuohy
needle and catheter direction in thoracic epidural anesthesia. Reg Anesth Pain Med
2006;31:105–12 Bibliographic Links [Context Link]
73. Hendriks GW, Hasenbos MA, Gielen MJ, van Egmond J, Barentz JO. Evaluation of
thoracic epidural catheter position and migration using radio-opaque catheters.
Anaesthesia 1997;52:457–9 Ovid Full Text Bibliographic Links [Context Link]
74. Beilin Y, Bernstein HH, Zucker-Pinchoff B. The optimal distance that a
multiorifice epidural catheter should be threaded into the epidural space. Anesth
Analg 1995;81:301–4 Ovid Full Text Bibliographic Links [Context Link]
75. D’Angelo R, Berkebile B, Gerancher JC. Prospective examination of epidural
catheter insertion. Anesthesiology 1996;84: 88–93 Ovid Full Text Bibliographic Links
[Context Link]
76. Hogan Q. Epidural catheter tip position and distribution of injectate evaluated by
computed tomography. Anesthesiology 1999;90:964–70 Ovid Full Text Bibliographic
Links [Context Link]
77. Husain FJ, Herman NL, Karuparthy VR, Knape KG, Downing JW. A comparison of
catheter vs needle injection of local anesthetic for induction of epidural anesthesia
for cesarean section. Int J Obstet Anesth 1997;6:101–6 Bibliographic Links [Context
Link]
78. Yun MJ, Kim YC, Lim YJ, Choi GH, Ha M, Lee JY, Ham BM. The differential flow
of epidural local anaesthetic via needle or catheter: a prospective randomized
double-blind study. Anaesth Intensive Care 2004;32:377–82 Bibliographic Links
[Context Link]
79. Omote K, Namiki A, Iwasaki H. Epidural administration and analgesic spread:
comparison of injection with catheters and needles. J Anesth 1992;6:289–93
Bibliographic Links [Context Link]
80. Crochetière CT, Trépanier CA, Cotè JJ. Epidural anaesthesia for caesarean
section: comparison of two injection techniques. Can J Anaesth 1989;36:133–6
Bibliographic Links [Context Link]
81. Power I, Thorburn J. Differential flow from multihole epidural catheters.
Anaesthesia 1988;43:876–8 Bibliographic Links [Context Link]
82. Segal S, Eappen S, Datta S. Superiority of multi-orifice over single-orifice
epidural catheters for labor analgesia and cesarean section. J Clin Anesth
1997;9:109–12 Bibliographic Links [Context Link]
83. D’Angelo R, Foss ML, Livesay CH. A comparison of multiport and uniport epidural
catheters in laboring patients. Anesth Analg 1997;84:1276–9 Ovid Full Text
Bibliographic Links [Context Link]
84. Michael S, Richmond MN, Livesay CH. A comparison between open end (single
hole) and closed end (three lateral holes) epidural catheters. Anaesthesia
1988;44:78–80 [Context Link]
85. Morrison LM, Buchan AS. Comparison of complications associated with singleholed and multi-holed extradural catheters. Br J Anaesth 1990;64:183–5 Bibliographic
Links [Context Link]
86. Magides AD, Sprigg A, Richmond MN. Lumbar epidurography with multi-orifice
and single-orifice catheters. Anaesthesia 1996;51:757–63 Ovid Full Text Bibliographic
Links [Context Link]
87. Jaime F, Mandell GL, Vallejo MC, Ramanathan S. Uniport soft-tip, open-ended
catheters versus multiport firm-tipped close-ended catheters for epidural labor
analgesia: a quality assurance study. J Clin Anesth 2000;12:89–93 Bibliographic Links
[Context Link]
88. Banwell BR, Morley-Forster P, Krause R. Decreased incidence of complications in
parturients with the Arrow (Flex Tip Plus) epidural catheter. Can J Anaesth
1998;45:370–2 [Context Link]
89. Okutomi T, Hashiba MM, Hashiba S, Masubuchi A, Morishima HO. The effects of
single and fractionated doses of mepivacaine on the extent of thoracic epidural
block. Reg Anesth Pain Med 2001;26:450–5 Bibliographic Links [Context Link]
90. Okutomi T, Minakawa M, Hoka S. Saline volume and local anesthetic
concentration modify the spread of epidural anesthesia. Can J Anaesth 1999;46:930–
4 Bibliographic Links [Context Link]
91. Okutomi T, Hoka S. Saline-anesthetic interval and the spread of epidural
anesthesia. Can J Anaesth 1999;46:935–8 Bibliographic Links [Context Link]
92. Kanai A, Suzuki A, Hoka S. Rapid injection of epidural mepivacaine speeds the
onset of nerve blockade. Can J Anaesth 2005;52:281–4 Bibliographic Links [Context
Link]
93. Griffiths RB, Horton WA, Jones IG, Blake D. Speed of injection and spread of
bupivacaine in the epidural space. Anaesthesia 1987;42:160–3 Bibliographic Links
[Context Link]
94. Hirabayashi Y, Matsuda I, Inoue S, Shimizu R. Epidural pressure and its relation to
spread of epidural analgesia. J Anesth 1987;1:168–72 Bibliographic Links [Context
Link]
95. Visser WA, Gielen MJM, Giele JL, Scheffer GJ. Comparison of epidural pressures
and incidence of true subatmospheric pressure between the mid-thoracic and lowthoracic epidural space. Anesth Analg 2006;103:1318–21 Ovid Full Text Bibliographic
Links [Context Link]
96. Bengis RG, Guyton AC. Some pressure and fluid dynamic characteristics of the
canine epidural space. Am J Physiol 1977;232:H255–H259 Bibliographic Links [Context
Link]
97. Shah JL. Influence of cerebrospinal fluid on epidural pressure. Anaesthesia
1981;36:627–31 Bibliographic Links [Context Link]
98. Telford RJ, Hollway TE. Observations on deliberate dural puncture with a Tuohy
needle: pressure measurements. Anaesthesia 1991;46:725–7 Bibliographic Links
[Context Link]
99. Okutomi T, Watanabe S, Goto F. Time course in thoracic epidural pressure
measurement. Can J Anaesth 1993;40:1044–8 Bibliographic Links [Context Link]
100. Zarzur E. Genesis of the ‘true’ negative pressure in the lumbar epidural space.
Anaesthesia 1984;39:1101–4 Bibliographic Links [Context Link]
101. Usubiaga JE, Moya F, Usubiaga LE. Effect of thoracic and abdominal pressure
changes on the epidural space pressure. Br J Anaesth 1967;39:612–8 Bibliographic
Links [Context Link]
102. Cardoso MM, Carvalho JC. Epidural pressures and spread of 2% lidocaine in the
epidural space: influence of volume and speed of injection of the local anesthetic
solution. Reg Anesth Pain Med 1998;23:14–9 Bibliographic Links [Context Link]
103. Paul DL, Wildsmith JAW. Extradural pressure following the injection of two
volumes of bupivacaine. Br J Anaesth 1989;62:368–72 Bibliographic Links [Context
Link]
104. Visser WA, Gielen MJM, Giele JLP. Continuous positive airway pressure
breathing increases spread of sensory blockade after low-thoracic injection of
lidocaine. Anesth Analg 2006;102:268–71 Ovid Full Text Bibliographic Links [Context
Link]
105. Visser WA, van Eerd MJPG, van Seventer R, Gielen MJM, Giele JL, Scheffer GJ.
Continuous positive airway pressure breathing increases cranial spread of sensory
blockade after cervico-thoracic injection of lidocaine. Anesth Analg 2007;105:868–71
Ovid Full Text Bibliographic Links [Context Link]
106. Ogura A, Yoshikawa T, Ikeda K, Inoue T. Time course of epidural pressure
change under intraperitoneal insufflation during laparoscopic surgery. Masui
1997;46:484–91 Bibliographic Links [Context Link]
107. Iwama H, Ohmori S. Continuous monitoring of lower thoracic epidural pressure.
J Crit Care 2000;15:60–3 Buy Now Bibliographic Links [Context Link]
108. Kaneko T, Iwama H. The association between injected volume of local
anesthetic and spread of epidural anesthesia: a hypothesis. Reg Anesth Pain Med
1999;24:153–7 Bibliographic Links [Context Link]
109. Iwama H, Ohmizo H, Kaneko T. Estimation of spread of lumbar or lower thoracic
epidural anesthesia by a simple equation. J Anesth 2000;14:224–5 Bibliographic Links
[Context Link]
110. Nakayama M, Yamamoto J, Ichinose H, Yamamoto S, Kanaya N, Namiki A.
Effects of volume and concentration of lidocaine on epidural anaesthesia in pregnant
females. Eur J Anaesthesiol 2002;19:808–11 Ovid Full Text Bibliographic Links
[Context Link]
111. Renck H, Edstrom H, Kinnberger B, Brandt G. Thoracic epidural analgesia-II:
prolongation in the early postoperative period by continuous injection of 1%
bupivacaine. Acta Anaesthesiol Scand 1976;20:47–56 Bibliographic Links [Context
Link]
112. Laveaux MM, Hasenbos MA, Harbers JB, Liem T. Thoracic epidural bupivacaine
plus sufentanil: high concentration/low volume versus low concentration/high
volume. Reg Anesth 1993;18:30–43 [Context Link]
113. Dernedde M, Stadler M, Bardiau F, Seidel L, Boogaerts JG. Low vs. high
concentration of levobupivacaine for postoperative epidural analgesia: influence of
mode of delivery. Acta Anaesthesiol Scand 2006;50:613–21 Buy Now Bibliographic
Links [Context Link]
114. Dernedde M, Stadler M, Bardiau F, Boogaerts JG. Continuous epidural infusion
of large concentration/small volume versus small concentration/large volume of
levobupivacaine for postoperative analgesia. Anesth Analg 2003;96:796–801 Ovid Full
Text Bibliographic Links [Context Link]
115. Scott DA, Chamley DM, Mooney PH, Deam RK, Mark AH, Häglöff B. Epidural
ropivacaine infusion for postoperative analgesia after major lower abdominal
surgery–a dose finding study. Anesth Analg 1995;81:982–6 Ovid Full Text Bibliographic
Links [Context Link]
116. Dernedde M, Nuyens V, Stadler M, Boogaerts JG. Comparison of two
concentrations of levobupivacaine for postoperative continuous epidural analgesia.
Anesthesiology 2006;105:A93 [Context Link]
117. Dernedde M, Stadler M, Bardiau F, Boogaerts JG. Comparison of different
concentrations of levobupivacaine for post-operative epidural analgesia. Acta
Anaesthesiol Scand 2003;47:884–90 Buy Now Bibliographic Links [Context Link]
118. Pittoni G, Mangano A, Arcidiacono S, Aiello L, Perona J. Post-operative
analgesia: effectiveness of different concentrations of epidural levobupivacaine.
Anesthesiology 2006; 105:A1631 [Context Link]
119. Liu SS, Ware PD, Rajendran S. Effects of concentration and volume of 2chloroprocaine on epidural anesthesia in volunteers. Anesthesiology 1997;86:1288–93
Ovid Full Text Bibliographic Links [Context Link]
120. Snijdelaar DG, Hasenbos MA, van Egmond J, Wolff AP, Liem TH. High thoracic
epidural sufentanil with bupivacaine: continuous infusion of high volume versus low
volume. Anesth Analg 1994;78:490–4 Ovid Full Text Bibliographic Links [Context Link]
121. Sakura S, Sumi M, Kushizaki H, Saito Y, Kosaka Y. Concentration of lidocaine
affects intensity of sensory block during lumbar epidural anesthesia. Anesth Analg
1999;88:123–7 Ovid Full Text Bibliographic Links [Context Link]
122. Kanai A, Hoka S. A comparison of epidural blockade produced by plain 1%
lidocaine and 1% lidocaine prepared by dilution of 2% lidocaine with the same
volume of saline. Anesth Analg 2006;102:1851–5 Ovid Full Text Bibliographic Links
[Context Link]
123. Strobel GE, Bianchi CP. The effects of pH gradients on the action of procaine
and lidocaine in intact and desheathed sciatic nerves. J Pharmacol Exp Ther
1970;172:1–17 Bibliographic Links [Context Link]
124. Strobel GE, Bianchi CP. The effects of pH gradients on the uptake and
distribution of C14-procaine and lidocaine in intact and desheathed sciatic nerve
trunks. J Pharmacol Exp Ther 1970;172:18–32 Bibliographic Links [Context Link]
125. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Lauber R, Högström H,
Scaramozzino P, Luginbühl M, Sieber TJ, Zbinden AM. Adding sodium bicarbonate to
lidocaine enhances the depth of epidural blockade. Anesth Analg 1998;86:341–7 Ovid
Full Text Bibliographic Links [Context Link]
126. Arakawa M, Aoyama Y, Ohe Y. Block of the sacral segments in lumbar epidural
anaesthesia. Br J Anaesth 2003;90:173–8 Ovid Full Text Bibliographic Links [Context
Link]
127. Arakawa M, Aoyama Y, Ohe Y. Epidural bolus injection with alkalinized
lidocaine improves blockade of the first sacral segment-a brief report. Can J Anaesth
2002;49:566–70 Bibliographic Links [Context Link]
128. Yaksh TL. Pharmacology of spinal adrenergic systems which modulate spinal
nociceptive processing. Pharmacol Biochem Behav 1985;22:845–58 Bibliographic Links
[Context Link]
129. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Fischer M, Zbinden AM. Epidural
epinephrine and clonidine. Segmental analgesia and effects on different pain
modalities. Anesthesiology 1997;87:785–94 Ovid Full Text Bibliographic Links
[Context Link]
130. Murphy TM, Mather LE, Stanton-Hicks M D’A, Bonica JJ, Tucker GT. The effects
of adding adrenaline to etidocaine and lignocaine in extradural anaesthesia I: block
characteristics and cardiovascular effects. Br J Anaesth 1976;48:893–8 Bibliographic
Links [Context Link]
131. Kopacz DJ, Helman JD, Nussbaum CE, Hsiang JNK, Nora PC, Allen HW. A
comparison of epidural levobupivacaine 0.5% with or without epinephrine for lumbar
spine surgery. Anesth Analg 2001;93:755–60 Ovid Full Text Bibliographic Links
[Context Link]
132. De Leon-Casasola OA, Lema MJ. Postoperative epidural opioids: what are the
choices? Anesth Analg 1996;83:867–75 Ovid Full Text Bibliographic Links [Context
Link]
133. Ginosar Y, Riley ET, Angst MS. The site of action of epidural fentanyl in humans:
the difference between infusion and bolus administration. Anesth Analg
2003;97:1428–38 Ovid Full Text Bibliographic Links [Context Link]
134. Kaneko M, Saito Y, Kirihara Y, Collins JG, Kosaka Y. Synergistic antinociceptive
interaction after epidural coadministration of morphine and lidocaine in rats.
Anesthesiology 1994;80:137–50 Buy Now Bibliographic Links [Context Link]
135. Vercauteren M, Meert TF. Isobolographic analysis of the interaction between
epidural sufentanil and bupivacaine in rats. Pharmacol Biochem Behav 1997;58:237–
42 Bibliographic Links [Context Link]
136. Cherng CH, Yang CP, Wong CS. Epidural fentanyl speeds the onset of sensory
and motor blocks during epidural ropivacaine anesthesia. Anesth Analg
2005;101:1834–7 Ovid Full Text Bibliographic Links [Context Link]
137. Joris JL, Jacob EA, Sessler DI, Deleuse J-FJ, Kaba A, Lamy ML. Spinal
mechanisms contribute to analgesia produced by epidural sufentanil combined with
bupivacaine for postoperative analgesia. Anesth Analg 2003;97:1446–51 Ovid Full
Text Bibliographic Links [Context Link]
138. Williams JP. Thoracic epidural anesthesia for cardiac surgery. Can J Anaesth
2002;49:R1–R6 [Context Link]
139. Carli F, Kehlet H. Continuous epidural analgesia for colonic surgery–but what
about the future? Reg Anesth Pain Med 2005;30:140–2 [Context Link]
140. Sielenkämper AW, van Aken H. Thoracic epidural anesthesia, more than just
anesthesia/analgesia. Anesthesiology 2003; 99:523–5 Ovid Full Text Bibliographic
Links [Context Link]
141. Veering BT, Cousins MJ. Cardiovascular and pulmonary effects of epidural
anaesthesia. Anaesth Intensive Care 2000; 28:620–35 [Context Link]
142. Brull SJ, Greene NM. Zones of differential sensory block during extradural
anaesthesia. Br J Anaesth 1991;66:651–5 Bibliographic Links [Context Link]
143. Peters J, Kousulis L, Arndt J. Effects of segmental thoracic extradural analgesia
on sympathetic block in conscious dogs. Br J Anaesth 1989;63:470–6 Bibliographic
Links [Context Link]
144. Hopf H-B, Weiszbach B, Peters J. High thoracic segmental epidural anesthesia
diminishes sympathetic outflow to the legs, despite restriction of sensory blockade
to the upper thorax. Anesthesiology 1990;73:882–9 Buy Now Bibliographic Links
[Context Link]
145. Magnusdottir H, Kirnö K, Ricksten S-E, Elam M. High thoracic epidural
anesthesia does not inhibit sympathetic nerve activity in the lower extremities.
Anesthesiology 1999;91:1299–304 Ovid Full Text Bibliographic Links [Context Link]
146. Baron J-F, Payen D, Coriat P, Edouard A, Viars P. Forearm vascular tone and
reactivity during lumbar epidural anesthesia. Anesth Analg 1988;67:1065–70
Bibliographic Links [Context Link]
147. Tanaka M, Goyagi T, Kimura T, Nishikawa T. The effects of cervical and lumbar
epidural anesthesia on heart rate variability and spontaneous sequence baroreflex
sensitivity. Anesth Analg 2004;99:924–9 Ovid Full Text Bibliographic Links [Context
Link]
148. Curatolo M, Scaramozzino P, Venuti FS, Orlando A, Zbinden AM. Factors
associated with hypotension and bradycardia after epidural blockade. Anesth Analg
1996;83:1033–40 Ovid Full Text Bibliographic Links [Context Link]
149. Kushizaki H, Doi K, Sakura S, Saito Y. High thoracic epidural anesthesia with
lidocaine, concentration and effect on pulmonary function. Anesthesiology
2005;103:A969 [Context Link]
150. Takasaki M, Takahashi T. Respiratory function during cervical and thoracic
epidural analgesia in patients with normal lungs. Br J Anaesth 1980;52:1271–6
Bibliographic Links [Context Link]
151. Barrington MJ, Kluger R, Watson R, Scott DA, Harris KJ. Epidural anesthesia for
coronary artery bypass surgery compared with general anesthesia alone does not
reduce biochemical markers of myocardial damage. Anesth Analg 2005; 100:921–8
Ovid Full Text Bibliographic Links [Context Link]
152. Abd Elrazek E, Scott NB, Vohra A. An epidural scoring scale for arm movements
(ESSAM) in patients receiving high thoracic epidural analgesia for coronary artery
bypass grafting. Anaesthesia 1999;54:1097–109 [Context Link]
153. Etches RC, Writer WDR, Ansley D, Nydahl PA, Ong BY, Lui A, Badner N, Kawolski
S, Muir H, Shukla R, Beattie WS. Continuous epidural ropivacaine 0.2% for analgesia
after lower abdominal surgery. Anesth Analg 1997;84:784–90 Ovid Full Text
Bibliographic Links [Context Link]
154. Murdoch JAC, Dickson UK, Wilson PA, Berman JS, Gad-Elrab RR, Scott NB. The
efficacy and safety of three concentrations of levobupivacaine administered as a
continuous epidural infusion in patients undergoing orthopedic surgery. Anesth Analg
2002;94:438–44 Ovid Full Text Bibliographic Links [Context Link]
155. Li Y, Zhu S, Bao F, Xu J, Yan X, Jin X. The effects of age on the median
effective concentration of ropivacaine for motor blockade after epidural anesthesia
with ropivacaine. Anesth Analg 2006;102:1847–50 Ovid Full Text Bibliographic Links
[Context Link]
156. Liu SS, Moore JM, Luo AM, Trautman WJ, Carpenter RL. Comparison of three
solutions of ropivacaine-fentanyl for postoperative patient controlled epidural
analgesia. Anesthesiology 1999;90:727–33 [Context Link]
157. Liu SS, Allen HW, Olsson GL. Patient-controlled epidural analgesia with
bupivacaine and fentanyl on hospital wards: prospective experience with 1030
surgical patients. Anesthesiology 1998;88:688–95 Ovid Full Text Bibliographic Links
[Context Link]
158. Schug SA, Scott DA, Payne J, Mooney PH, Hägglöf B. Postoperative analgesia by
continuous extradural infusion of ropivacaine after upper abdominal surgery. Br J
Anaesth 1996; 76:487–91 Bibliographic Links [Context Link]
159. Standl T, Burmeister M-A, Ohnesorge H, Wilhelm S, Striepke M, Gottschalk A,
Horn EP, Schulte Am Esch J. Patient-controlled epidural analgesia reduces analgesic
requirements compared to continuous epidural infusion after major abdominal
surgery. Can J Anaesth 2003;50:258–64 Bibliographic Links [Context Link]
160. Salvi L, Sisillo E, Brambillasca C, Juliano G, Salis S, Marino MR. High thoracic
epidural anesthesia for off-pump coronary artery bypass surgery. J Cardiothorac Vasc
Anesth 2004;18:256–62 Bibliographic Links
161. Liem TH, Booij LHDJ, Hasenbos MAWM, Gielen MJM. Coronary artery bypass
grafting using two different anesthetic techniques: part I: hemodynamic results. J
Cardiothorac Vasc Anesth 1992;6:148–55 Bibliographic Links
162. Goertz AW, Seeling W, Heinrich H, Lindner KH, Schirmer U. Influence of high
thoracic epidural anesthesia on left ventricular contractility assessed using the endsystolic pressure-length relationship. Acta Anaesthesiol Scand 1993;37:38–44
Bibliographic Links
163. Licker M, Spiliopoulos A, Tschopp JM. Influence of thoracic epidural analgesia
on cardiovascular autonomic control after thoracic surgery. Br J Anaesth
2003;91:525–31 Ovid Full Text Bibliographic Links
164. Senard M, Joris JL, Ledoux D, Toussaint PJ, Lahaye-Goffart B, Lamy ML. A
comparison of 0.1% and 0.2% ropivacaine and bupivacaine combined with morphine
for patient-controlled epidural analgesia after major abdominal surgery. Anesth
Analg 2002;95:444–9 Ovid Full Text Bibliographic Links